Oncotarget

Research Papers:

The impact of RNA binding motif protein 4-regulated splicing cascade on the progression and metabolism of colorectal cancer cells

Yu-Chih Liang _, Wei-Cheng Lin, Ying-Ju Lin and Jung-Chun Lin

PDF  |  HTML  |  Supplementary Files  |  How to cite  |  Order a Reprint

Oncotarget. 2015; 6:38046-38060. https://doi.org/10.18632/oncotarget.5710

Metrics: PDF 902 views  |   HTML 1083 views  |   ?  


Abstract

Yu-Chih Liang1,*, Wei-Cheng Lin2,*, Ying-Ju Lin3, Jung-Chun Lin1

1School of Medical Laboratory Science and Biotechnology, College of Medical Science and Technology, Taipei Medical University, Taipei, Taiwan

2Division of Thoracic Surgery, Wan Fang Hospital, Taipei Medical University, Taipei, Taiwan

3School of Chinese Medicine, China Medical University, Taichung, Taiwan

*These authors have contributed equally to this work

Correspondence to:

Jung-Chun Lin, e-mail: lin2511@tmu.edu.tw

Keywords: alternative splicing, colorectal cancer, miR-92a, nPTB, RBM4

Received: July 14, 2015     Accepted: October 06, 2015     Published: October 19, 2015

ABSTRACT

Dysregulated splicing of pre-messenger (m)RNA is considered a molecular occasion of carcinogenesis. However, the underlying mechanism is complex and remains to be investigated. Herein, we report that the upregulated miR-92a reduced the RNA-binding motif 4 (RBM4) protein expression, leading to the imbalanced expression of the neuronal polypyrimidine tract-binding (nPTB) protein through alternative splicing-coupled nonsense mediated decay (NMD) mechanism. Increase in nPTB protein enhances the relative level of fibroblast growth factor receptor 2 IIIc (FGFR2) and pyruvate kinase M2 (PKM2) transcripts which contribute to the progression and metabolic signature of CRC cells. Expression profiles of RBM4 and downstream alternative splicing events are consistently observed in cancerous tissues compared to adjacent normal tissues. These results constitute a mechanistic understanding of RBM4 on repressing the carcinogenesis of colorectal cells.


Creative Commons License All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 3.0 License.
PII: 5710